Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes

Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperat...

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Bibliographic Details
Published in:Chinese journal of natural medicines 2017-03, Vol.15 (3), p.178-191
Main Authors: JIANG, Jing-Fei, LEI, Fan, YUAN, Zhi-Yi, WANG, Yu-Gang, WANG, Xin-Pei, YAN, Xiao-Jin, YU, Xuan, XING, Dong-Ming, DU, Li-Jun
Format: Article
Language:English
Subjects:
Animals
Berberine
Berberine - pharmacology
Heat Stress Disorders - drug therapy
Heat Stress Disorders - genetics
Heat Stress Disorders - metabolism
Hot Temperature
HSP70
HSP70 Heat-Shock Proteins - genetics
HSP70 Heat-Shock Proteins - metabolism
Humans
Hyperthermia
Male
Mice
Mice, Inbred ICR
TATA box
TATA Box - drug effects
TNFα
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - metabolism
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Summary:Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments.
ISSN:1875-5364
1875-5364
DOI:10.1016/S1875-5364(17)30034-1